Urinary Albumin Levels Research Articles

The relationship between water intake and the progression of urine albumin-creatinine ratio in patients with chronic kidney disease: A cohort-prospective study.

Introduction: The urine albumin-creatinine ratio (uACR) is a key biomarker for assessing kidney function in patients with chronic kidney disease (CKD), with elevated levels indicating kidney damage. Water and protein metabolism significantly impact kidney function. Proper hydration influences vasopressin feedback and osmolality regulation, while excessive protein intake exacerbates kidney stress through hyperfiltration and increased urea production. This study aims to investigate the relationship between daily water and protein intake and uACR levels in CKD patients. Methods: A cohort study was conducted on 10 non-dialysis CKD patients at Dr. Wahidin Sudirohusodo Hospital, Makassar, Indonesia. Demographic and clinical data were collected, and average daily water and protein intake were assessed. The Spearman correlation test was used to analyze the relationship between water and protein intake and changes in uACR, albumin, and creatinine levels. Results: A strong negative correlation was found between daily water intake and uACR (ρ=-0.891, p=0.001), indicating that higher water consumption reduces uACR. Conversely, protein intake showed a strong positive correlation with uACR (ρ=0.770, p=0.009) and urine albumin levels (ρ=0.806, p=0.005), suggesting that higher protein consumption increases both uACR and albumin excretion. No significant correlation was found between water or protein intake and urine creatinine levels. Conclusion: This study highlights the importance of hydration and dietary protein regulation in managing CKD progression. Increased water intake may reduce uACR, while excessive protein intake can exacerbate kidney damage, emphasizing the need for dietary management in CKD patients.

SA4503 Mitigates Adriamycin-Induced Nephropathy via Sigma-1 Receptor in Animal and Cell-Based Models

Background/Objectives: The Sigma-1 receptor (Sigmar1), an intracellular chaperone protein, is ubiquitously expressed throughout the body, but its role in peripheral organs, such as the kidneys, remains unclear. Here, we investigated the protective effects and molecular mechanisms of SA4503, a selective Sigmar1 agonist, on Adriamycin (ADR)-induced renal glomerular injury. Methods: Using in vitro and in vivo models, we evaluated the effects of SA4503 on ADR-induced podocyte injury, including podocyte survival, albumin permeability, urinary albumin levels, and Sigmar1-nephrin interactions. NE-100, a Sigmar1 antagonist, was co-administered to validate the specificity of the effects of SA4503. Results: Sigmar1 was highly expressed in podocytes and mouse kidney tissues. SA4503 significantly reduced ADR-induced podocyte injury and urinary albumin leakage in mice. Mechanistically, SA4503 preserved Sigmar1-nephrin interactions, which were disrupted in ADR-treated kidneys. This protective effect was abolished by NE-100 co-treatment, confirming the Sigmar1-dependency of SA4503’s action. Conclusions: These findings demonstrate that the activation of Sigmar1 by SA4503 protects against ADR-induced podocyte injury and glomerular damage, likely by stabilizing Sigmar1-nephrin interactions. Therefore, Sigmar1 represents a promising therapeutic target for glomerular diseases such as nephrotic syndrome.

Non-linear relationship between urinary creatinine and diabetic kidney disease: implications for clinical practice

ObjectiveThis study aims to investigate the relationship between urinary creatinine (UCr) and the risk and severity of Diabetic Kidney Disease (DKD) in patients with Type 2 Diabetes Mellitus (T2DM). The goal is to establish UCr as a potential biomarker for early DKD detection and severity assessment.MethodsA retrospective cross-sectional analysis was conducted using medical records of T2DM patients. Patients were classified into groups with and without DKD, and relevant clinical data, including demographic, blood, and urine parameters, were collected. Logistic regression and receiver operating characteristic (ROC) curve analysis evaluated the association between UCr levels and DKD. Curve fitting and threshold effect model were used to further evaluate the relationship between UCr and the incidence and severity of DKD.ResultsA total of 302 T2DM patients were analyzed, with 137 diagnosed with DKD. Significant differences in clinical parameters were observed between the DKD and non-DKD groups, particularly in UCr, urine albumin levels, and eGFR. UCr levels demonstrated a strong association with DKD. Moreover, a non-linear relationship was identified, with specific inflection points indicating different correlation patterns of UCr with DKD occurrence and progression.ConclusionThe findings of this study highlight the potential of UCr as a valuable biomarker for early detection and assessment of DKD in T2DM patients. Incorporating UCr measurements into routine clinical practice could enhance early identification of patients at risk for kidney complications, leading to timely intervention and improved patient outcomes.

Diagnosing alkaptonuria-related nephropathy with urine albumin analysis.

Homogentisic acid (HGA) accumulation in alkaptonuria (AKU) causes injuries in various organs including the kidney. We present a case of a 9-year-old girl initially diagnosed with AKU-related nephropathy due to proteinuria found in her urine analyses. Despite 1month of ramipril treatment, the patient's proteinuria progressed, and as a result, kidney biopsy and nitisinone treatment were planned. In addition, we controlled her proteinuria with urine albumin measurement. After finding a normal urine albumin level in the 24-h urine sample, we realized that the patient was misdiagnosed with proteinuria because of HGA interference with urine protein level measurement using benzethonium. The patient's treatment for kidney injury was canceled. Urine albumin level was measured as normal 2months later, confirming proteinuria was a false-positive test result. AKU-related nephropathy should be evaluated with urine albumin measurement instead of protein. In this way, the complication risk of unnecessary interventions and pharmacotherapies can be avoided.

Neutrophil-Lymphocyte Ratio as a Novel Biomarker for Diabetic Nephropathy in Type 2 Diabetes Mellitus Patients: A Cross-Sectional Study

Background: Early detection of diabetic nephropathy (DN) is crucial to prevent progression to end-stage renal disease. The gold standard for diagnosing DN involves urine microalbumin testing and renal biopsy. However, the availability of these diagnostic tools is limited in many healthcare facilities across Indonesia. Consequently, there is a pressing need for an alternative examination that is readily accessible and can effectively monitor the progression of DN. Methods: This cross-sectional study was conducted at Dr. Mohammad Hoesin General Hospital, Palembang, from February 2024 to May 2024. The study aimed to investigate the correlation between neutrophil-lymphocyte ratio (NLR) and urinary albumin levels in type 2 diabetes mellitus (DM) patients. NLR, calculated from complete blood counts, has emerged as a potential inflammatory marker for various conditions. A total of 65 participants diagnosed with type 2 DM were enrolled in the study. Data analysis involved Spearman's correlation test to assess the relationship between NLR and urinary albumin levels. Results: The majority of the 65 subjects were female (58.5%). The study found that 44 subjects had normoalbuminuria, 18 had microalbuminuria, and 3 had macroalbuminuria. A significant positive correlation was observed between NLR and albuminuria levels in type 2 DM patients (r = 0.795; p < 0.01). Conclusion: The study's findings suggest that NLR is a potential cost-effective biomarker for the early detection of DN in type 2 DM patients, especially in resource-limited settings. Further large-scale studies are recommended to validate these findings and establish specific NLR thresholds for predicting DN progression.

Interaction between 24 h Urinary Free Cortisol and Obesity in Hypertension-Mediated Organ Damage in Patients with Untreated Hypertension.

Given the close relationship between excessive cortisol secretion and obesity, as well as their intimate associations with cardiometabolic sequelae, this study aimed to evaluate whether elevated cortisol levels and obesity are independently and potentially interactively related to hypertension-mediated organ damage (HMOD) in patients with untreated hypertension. A total of 936 untreated hypertensive patients were recruited. Body mass index (BMI), 24-hour urinary free cortisol (24 h UFC), and HMOD indicators, including left ventricular hypertrophy (LVH), carotid intima-media thickness (CIMT), and albuminuria, were assessed. Multivariate logistic regression was conducted to evaluate the associations of HMOD indicators with 24 h UFC and obesity. Generalized linear models were used to test for the interaction effects of obesity in the associations between log 24 h UFC levels and HMOD indicators. Compared to non-obese patients, those who were obese had a greater left ventricular mass index (LVMI), greater CIMT, a higher level of 24-hour urinary albumin (24 h UALB) and more frequent albuminuria (all p < 0.05). In the obese group, elevated 24 h UFC was significantly associated with LVH (odds ratio (OR) = 2.53; 95% CI: 1.02-6.31, p = 0.044) and albuminuria (OR = 3.13; 95% CI: 1.31-7.43, p = 0.01), after multivariate adjusting. There was a significant interactive effect of obesity on the association between 24 h UFC and LVH and albuminuria (all p for interaction <0.05). A significant correlation was observed between 24 h UFC and LVMI in obese and non-obese patients. Conversely, the correlations of 24 h UFC and log 24 h UALB were found only in obese patients but not in non-obese patients. Elevated 24 h UFC levels were associated with higher severity of HMOD, including more frequent LVH, albuminuria, and greater CIMT. Additionally, obesity modified the effects of 24 h UFC on both LVH and albuminuria.

Unraveling diabetic kidney disease: insights from single-cell RNA sequencing.

The incidence of diabetic kidney disease (DKD) is rising annually. Diabetes leads to structural damage and dysfunction in the kidneys, clinically manifesting as progressive proteinuria and declining renal function, ultimately resulting in end-stage renal disease (ESRD). Recent findings have identified a subset of DKD known as normoalbuminuric diabetic kidney disease (NADKD), characterized by normal urine albumin levels but reduced renal function. These complex clinical presentations and underlying pathophysiology challenge traditional diagnostic and treatment approaches. Single-cell RNA sequencing (scRNA-seq), a novel experimental technique, is employed to analyze gene expression in renal tissue, blood, and urine from DKD patients, enhancing our understanding of tissue function, cellular interactions, and disease progression. This approach facilitates early screening and personalized management of DKD.

Association between hypertension duration and chronic kidney disease in residents in China

Objective: To evaluate the association between hypertension duration and risk for chronic kidney disease in residents in China. Methods: Participants aged 18-74 years from the sixth round of China Chronic Disease and Risk Factor Surveillance in 2018 were included. The age/date at hypertension diagnosis was reported by them, and hypertension duration was calculated based on the age at diagnosis and the age at survey. The hypertension duration was calculated as 0 year (i.e., normotensive participants), 0.1- year, 5.0- years, 10.0- years, and ≥15.0 years. Serum creatinine, urinary albumin, and urinary creatinine levels were measured, and chronic kidney disease was diagnosed when glomerular filtration rate was <60 ml·min-1·(1.73 m2)-1 and/or urine albumin-to-creatinine ratio was ≥30 mg/g. Multivariable logistic regression analysis, which took intra-group correlation into account, was used to evaluate the association of hypertension duration with chronic kidney disease. Results: A total of 140 662 residents were finally included in the analysis. After adjusting the confounders, including blood pressure, the odds ratio of chronic kidney disease was 1.16 (95%CI: 1.09-1.23), 1.33 (95%CI: 1.20-1.48), 1.33 (95%CI: 1.18-1.49), and 1.43 (95%CI: 1.29-1.60) in study subjects with hypertension durations of 0.1-4.9 years, 5.0-9.9 years, 10.0-14.9 years, and ≥15.0 years, respectively, in comparison with normotensive people. This result was further supported by the positive association between hypertension duration and chronic kidney disease in people with previously diagnosed hypertension. The results of restricted cubic spline suggested that the risk for chronic kidney disease showed a steep increase within 0.1- 4.9 years after hypertension diagnosis, then showed neither increase nor decrease. The above association seemed to be stronger in those with hypertension diagnosed age <45 years. Compared with those with hypertension duration of 0.1-4.9 years, the odds ratio was 1.38 (95%CI: 1.04-1.84), 1.22 (95%CI: 0.91-1.65), and 1.47 (95%CI: 1.04-2.07) in those with hypertension durations of 5.0-9.9 years, 10.0-14.9 years, and ≥15.0 year, respectively. In those with hypertension diagnosis at ≥45 years, the corresponding odds ratio was 1.08 (95%CI: 0.98-1.19), 1.08 (95%CI: 0.97-1.21), and 1.16 (95%CI: 1.02-1.32), respectively. Conclusions: Hypertension duration is positively associated with the risk for chronic kidney disease in residents in China, and this association is independent of blood pressure level. Early diagnosis of hypertension and long-term control of blood pressure are effective strategies for secondary prevention of hypertension-related chronic kidney disease.

Predictive Value and Potential of Targeting Complement Factor C3 in Patients with Renal Injury in Preeclampsia.

The activation of the complement system is accompanied by the occurrence and development of preeclampsia, as well as kidney diseases. Here, the role of complement C3 [C3] in renal injury in preeclampsia was explored, and its potential application as an early diagnostic biomarker or drug target to ameliorate kidney injury induced by preeclampsia was preliminarily evaluated. A total of 48 subjects were included in the present study, and the complement C3 levels and renal function were analyzed. Patients with preeclampsia with severe features [sPe] had poorer renal function compared with the patients with preeclampsia. Urinary C3 levels could be used to distinguish between healthy controls, patients with preeclampsia, and patients with sPe. Increased renal inflammation and oxidative stress were notably increased in the preeclampsia mice with impaired renal function and attenuation of C3 activity using a C3 receptor antagonist, which reduced Pe-like symptoms and renal impairment, decreased serum blood urea nitrogen, creatinine, and urinary albumin levels, and decreased expression of the oxidative stress marker malondialdehyde, whilst increasing superoxide dismutase activity. In addition, activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 ([HO-1) pathway was involved in the inhibition of complement C3 in the kidney. Higher urinary C3 levels could be used to predict kidney damage as it was found that the activation of the Nrf2/HO-1 pathway attenuated C3 levels, and this resulted in increased renal impairment in preeclampsia.

Sulforaphane alleviates membranous nephropathy by inhibiting oxidative stress-associated podocyte pyroptosis.

To investigate the natural product sulforaphane (SFN) in protection of membranous nephropathy (MN) by inhibiting oxidative stress-associated podocyte pyroptosis. A passive Heymann nephritis (PHN) model was established and treated with SFN. Clinical manifestations were examined by testing 24-hr urine protein, albumin, total cholesterol, triglyceride, high-density and low-density lipoprotein levels. Podocyte injury was observed through glomerular ultrastructure and the expression of podocin and desmin. Intrarenal oxidative stress was evaluated through assessment of oxidative markers, including malondialdehyde, 8-isoprostane, and 8-hydroxydeoxyguanosine, and the activities of anti-oxidant enzymes, including total superoxide dismutase, catalase, and γ-glutamylcysteine synthetase. Podocyte and intrarenal pyroptosis were investigated by observing the localization of the GSDMD N-terminus (GSDMD(N)) in podocytes; the expression of pyroptosis signaling pathway, including GSDMD, NF-κB p65, p-NF-κB p65 (Ser536), NLRP3, ASC, caspase-1, IL-1β, and IL-18; and pyroptosis encounter Nrf2 in the glomeruli and kidney. SFN has a protective effect on MN, as reflected by alleviation of nephrotic syndrome, amelioration of podocyte foot process fusion, increased expression and normalization of podocin, and decreased expression of desmin in the glomeruli. Mechanistically, SFN relieved intrarenal oxidative stress, as indicated by decreased renal malondialdehyde, 8-isoprostane, and 8-hydroxydeoxyguanosine and increased activity of total superoxide dismutase, catalase, and γ-glutamylcysteine synthetase. SFN also inhibited podocyte and intrarenal pyroptosis, as revealed by decreased colocalization of GSDMD (N) with synaptopodin and ZO-1, decreased expression of pyroptosis signaling pathway, and increased expression of Nrf2 in the glomeruli and kidney. SFN could alleviate MN by inhibiting oxidative stress-associated podocyte pyroptosis.

Astragaloside for Improving Diabetic Vasculopathy Based on Microalbuminuria and C-Reactive Protein

Astragaloside has an ameliorative effect on diabetic vasculopathy. In this experiment, we investigated the role of astragaloside in improving diabetic vasculopathy. Eighty cases of type 2 diabetes mellitus (T2DM) patients with microalbuminuria (MAU) symptoms were selected and divided into T2DM group, astragaloside group, astragaloside+SRI-011381 group and astragaloside+ LDN193189 group. Another 20 healthy check-ups were selected as control group. We detected the content of C-reactive protein (CRP), ankle-brachial index (ABI) for both lower limbs, ultrasound examination of both lower limbs, and determined the vascular internal diameter (D), peak flow rate (Vmax), blood flow (Vol) of these three arteries, as well as grading the degree of lesion and scoring. T2DM group showed an increase in CRP level and UAlb content, decreased vessel internal diameter, an increased peak flow rate, decreased blood flow and ABI index, and a higher incidence of arteriopathy, which were all reversed in the Astragaloside group. The incidence of arterial lesions was lower. Compared with astragaloside group, serum CRP level and urine albumin content were increased in the astragaloside+SRI-011381 group, and serum CRP level and urine albumin content were decreased in the astragaloside+LDN193189 group. Moreover, inhibition of TGF-β/Smad pathway improved diabetic vasculopathy. Astragaloside therefore improves diabetic vasculopathy and slows diseased progression by inhibiting TGF-β/Smad signaling, lowering CRP levels as well as urinary albumin levels, hindering vasoconstriction and increasing blood flow.

Moringa isothiocyanate-1 mitigates the damage of oxidative stress and apoptosis in diabetic nephropathy mice.

Diabetic nephropathy (DN) is a prevalent cause of end-stage kidney disease worldwide. Moringa isothiocyanate-1 (MIC-1) has shown potential for DN management, however, the exact mechanisms remain unclear. This research intended to evaluate the impact and mechanism of MIC-1 on DN. Six C57BLKS/J-db/m mice served as controls. Eighteen C57BLKS/J-db/db mice were randomly separated into three groups: db/db, db/db + irbesartan (IBS), and db/db + MIC-1. Three weeks post-drug administration, the body weight and kidney weight of mice in each group were measured. Concurrently, serum creatinine (Scr), urine albumin, insulin, glycosylated hemoglobin (GHb), oxidative stress-, and inflammatory-related factors were determined. Additionally, the pathological injury, apoptosis, apoptosis-related markers, NLRP3, and ASC levels in the kidney tissues were examined utilizing H&E, Masson, PAS, TUNEL staining, and Western blot. MIC-1 decreased the body weight, kidney weight, the levels of Glu, Scr, and urine albumin in db/db mice. Moreover, MIC-1 significantly suppressed the levels of MDA, insulin, GHb, TNF-α, IL-1β, and IL-6, while increased the activities of SOD, CAT, and GPX in the serum of db/db mice. MIC-1 also mitigated the kidney tissue injury in db/db mice. Western blot assay showed that MIC-1 enhanced the Bcl-2 level and suppressed the Bax, cleaved caspase-3, cleaved caspase-9, NLRP3, ASC, and caspase-1 levels of the kidney tissues in db/db mice. MIC-1 ameliorated the kidney injury in DN mice, and its mechanism may be associated with the suppression of renal cell apoptosis, oxidative stress, and inflammatory responses.

Loss of the Endothelial Glycocalyx Component EMCN Leads to Glomerular Impairment.

EMCN (endomucin), an endothelial-specific glycocalyx component, was found to be highly expressed by the endothelium of the renal glomerulus. We reported an anti-inflammatory role of EMCN and its involvement in the regulation of VEGF (vascular endothelial growth factor) activity through modulating VEGFR2 (VEGF receptor 2) endocytosis. The goal of this study is to investigate the phenotypic and functional effects of EMCN deficiency using the first global EMCN knockout mouse model. Global EMCN knockout mice were generated by crossing EMCN-floxed mice with ROSA26-Cre mice. Flow cytometry was used to analyze infiltrating myeloid cells in the kidneys. The ultrastructure of the glomerular filtration barrier was examined by transmission electron microscopy, whereas urinary albumin, creatinine, and total protein levels were analyzed from freshly collected urine samples. Expression and localization of EMCN, EGFP, CD45, CD31, CD34, podocin, and albumin were examined by immunohistochemistry. Mice were weighed regularly, and their systemic blood pressure was measured using a noninvasive tail-cuff system. Glomerular endothelial cells and podocytes were isolated by fluorescence-activated cell sorting for RNA sequencing. Transcriptional profiles were analyzed to identify differentially expressed genes in both endothelium and podocytes, followed by gene ontology analysis. Protein levels of EMCN, albumin, and podocin were quantified by Western blot. The EMCN-/- mice exhibited increased infiltration of CD45+ cells, with an increased proportion of Ly6GhighLy6Chigh myeloid cells and higher VCAM-1 (vascular cell adhesion molecule 1) expression. EMCN-/- mice displayed albuminuria with increased albumin in the Bowman's space compared with the EMCN+/+ littermates. Glomeruli in EMCN-/- mice revealed fused and effaced podocyte foot processes and disorganized endothelial fenestrations. We found no significant difference in blood pressure between EMCN knockout mice and their wild-type littermates. RNA sequencing of glomerular endothelial cells revealed downregulation of cell-cell adhesion and MAPK (mitogen-activated protein kinase)/ERK (extracellular signal-regulated kinase) pathways, along with glycocalyx and extracellular matrix remodeling. In podocytes, we observed reduced VEGF signaling and alterations in cytoskeletal organization. Notably, there was a significant decrease in both mRNA and protein levels of podocin, a key component of the slit diaphragm. Our study demonstrates a critical role of the endothelial marker EMCN in supporting normal glomerular filtration barrier structure and function by maintaining glomerular endothelial tight junction and homeostasis and podocyte function through endothelial-podocyte crosstalk.

Renal tubular damage as an independent risk factor for all-cause and cardiovascular mortality in a community-based population: the Takahata study.

Renal tubular damage plays a crucial role in the development of end-stage kidney disease, a risk factor for cardiovascular events and mortality. However, the relationship between renal tubular damage and all-cause and cardiovascular mortality rates in the general population remains unclear. To address this gap, we conducted a cohort study in the general population using the urinary β2-microglobulin-creatinine ratio (UBCR) as a marker of renal tubular damage. This study included 3427 residents aged ≥ 40years in Takahata, Japan. We examined the association between the UBCR values in single-spot urine samples at enrollment and all-cause and cardiovascular mortality rates within a median follow-up of 9.2years. The participants were divided into two groups based on their UBCR levels (< 300μg/g and ≥ 300μg/g groups). Kaplan-Meier analysis showed a significantly higher incidence of all-cause and cardiovascular mortality rates in the high UBCR group (log-rank P < 0.01). Multivariable Cox proportional hazards model adjusted for age, sex, estimated glomerular filtration rate (eGFR), urine albumin level, smoking, and comorbidities showed a significantly higher hazard ratio of 1.49 (95% confidence interval (CI) 1.10-2.03, P = 0.01) for all-cause mortality and a hazard ratio of 1.73 (95% CI 1.00-2.98, P = 0.048) for cardiovascular mortality in the high-UBCR group. The net reclassification index was significantly improved by adding a high UBCR to the conventional risk factors. UBCR is an independent risk factor for all-cause and cardiovascular mortality in the general population, independent of eGFR and urinary albumin levels.

Topiroxostat-A Safer Uricostatic Drug with Enhanced Renal Protection: A Narrative Review.

Background: Topiroxostat, a selective xanthine oxidase inhibitor, effectively reduces serum urate levels in hyperuricemia patients with or without gout. The present narrative review aims to evaluate the existing evidence regarding the effectiveness of topiroxostat on renal function in patients with and without kidney disease. Materials and methods: A systematic search was conducted to identify relevant studies on renal function and topiroxostat published between 2005 and 2023. Various electronic databases were searched using different combinations of medical subject headings (MeSH) terms, and cross-referencing was performed. A total of 3146 articles were retrieved, and 18 met the inclusion and exclusion criteria. Results: The review included 18 studies investigating the effectiveness of topiroxostat on renal function in patients with and without kidney disease. Topiroxostat demonstrated maintenance of renal function, as evidenced by stable levels of estimated glomerular filtration rate (eGFR), serum creatinine, urinary albumin, and urinary protein. Furthermore, topiroxostat led to improvements in renal function, including increased eGFR and decreased levels of urinary albumin, uric acid, urinary protein, urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), and liver-type fatty acid-binding protein (L-FABP) following treatment. The literature also supports the safety profile of topiroxostat. Conclusion: Topiroxostat shows promise as an efficient and safe renoprotective agent in patients, irrespective of renal disease status. However, further large-scale, long-term, and multicenter clinical studies are needed to generate high-quality evidence in different populations and settings.

Gender-associated features in diabetic kidney disease

Diabetic kidney disease (DKD) is the leading cause of end-stage renal failure. Evidence indicates gender differences in the progression of this disease. This study aimed to determine gender differences in prevalence and identify gender-associated risk factors contributing to the development of diabetic kidney disease in individuals with type 2 diabetes mellitus (T2DM). The cross-sectional study included 132 patients with T2DM ranging in age from 50 to 65 years. Subjects were stratified by sex (80 women and 52 men). Gender differences have been studied in relation to the incidence and prevalence of DKD, their phenotypes and clinical manifestations, and several risk factors that have different effects on both sexes. The outcome of clinical kidney function assessment showed that 70% subjects were diagnosed with DKD (71% of women and 67% of men). The study indicated an association between the duration of T2DM and urinary albumin levels, as well as between arterial hypertension and triglyceride levels, which are independent risk factors for DKD development. Notably, older women with T2DM have a higher prevalence of DKD than older men. The albuminuric component of DKD was more frequently observed in men. Additionally, men were more likely to have adverse risk factors, including dyslipidemia, lower high-density lipoprotein cholesterol, and glomerular filtration rate, which are factors involved in the mechanisms of DKD. In summary, the results indicate that: 1) women with type 2 diabetes mellitus are at a higher risk of developing a normoalbuminuric phenotype of diabetic kidney disease, while men are at a higher risk of developing an albuminuric phenotype of diabetic kidney disease leading to renal failure and end-stage renal disease; 2) gender differences are most noticeable among older adults and may have significant implications for the development of more effective diagnostic and treatment methods for diabetic kidney disease, tailored to individual needs.

Relationship between serum level of miR-338-3p and miR-105-3p and bone metabolic markers in patients with diabetes nephropathy

Objectives Diabetic nephropathy (DN) is one of the most common and serious complications of diabetes. The purpose of this study was to explore the relationship between serum microRNA-338-3p (miR-338-3p) and miR-105-3p and bone metabolic markers in patients with DN at different stages. Methods A total of 153 patients diagnosed and treated in the Department of Nephrology from July 2020 to October 2021 were selected as the study objects. According to the staging criteria of diabetic nephropathy and 24-h urinary albumin quantitative level, the patients were divided into control group (35 cases), microalbuminuria group (37 cases), clinical stage albuminuria group (27 cases) and renal failure group (54 cases). Gene expressions were measured by real-time fluorescence quantitative PCR. The correlation was analyzed by Spearman. Serum miR-338-3p and miR-150-5p in the prediction of renal failure in DN was analyzed by ROC curve. Results The levels of urinary albumin and serum creatinine were markedly increased with the increase of DN stage (p < 0.05). Compared with the microalbuminuria group, the expression levels of serum miR-383-3p, serum miR-105-3p, 25(OH)-D, BGP and PINP were obviously decreased, but the expression of parathyroid hormone (PTH) and type I collagen (β-CTX) was largely increased in clinical proteinuria group (p < 0.05). Compared with the clinical proteinuria group, the expression levels of serum miR-383-3p, serum miR-105-3p, 25(OH)-D, BGP and PINP were largely decreased, but the expression of PTH and β-CTX was obviously increased in the renal failure group (p < 0.05). Spearman correlation results showed that serum expressions of miR-383-3p and miR-105-3p were negatively correlated with PTH and β-CTX, and positively correlated with 25(OH)-D, BGP and PINP (p < 0.05). ROC curve analysis showed that the AUC of serum miR-338-3p and miR-150-5p was 0.896 with the specificity and sensitivity of 96.66% and 73.47%, which had certain predictive value for the occurrence of renal failure in DN. Conclusions The expression levels of serum miR-383-3p and miR-105-3p were significantly correlated with bone metabolism markers. The combined test can provide new ideas and insights for the clinical treatment of osteoporosis in DN.

Comparison of Thyroid Function Tests Among Type 2 Diabetes Patients With and Without Diabetic Nephropathy and Controls.

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder associated with hyperglycemia and impaired insulin function. Diabetic nephropathy (DN) is a common complication of T2DM, characterized by progressive kidney damage. Thyroid dysfunction, particularly hypothyroidism, has been increasingly recognised as a significant factor influencing the progression of DN. To compare thyroid function tests in patients with T2DM with and without diabetic nephropathy and non-diabetic controls, and to assess the role of thyroid dysfunction in DN progression. A hospital-based cross-sectional study was conducted among 225 participants. Patients were divided into three groups: T2DM with DN, T2DM without DN, and controls, with 75 participants in each group. Data collection included demographic details, comorbidities, and clinical assessments such as blood pressure, thyroid function tests, urinary albumin levels, glycated hemoglobin (HbA1c), renal function tests, serum electrolytes, and estimated glomerular filtration rate (eGFR). Statistical analyses were conducted using SPSS version 20.0 (IBM Corp., Armonk, NY, USA). Results:The most common DN stage among T2DM patients was stage 4 (29, 38.7%), followed by stages 2 and 5 (19, 25.3%each). The T2DM with DN (47, 62.7%) group had a higher prevalence of overweight and obesity compared to the T2DM without DN group (38, 51.5%) and controls (24, 32%) (p value<0.001). Abnormal cardiovascular, respiratory, and abdominal examinations were most prevalent in the T2DM with DN group. Hypothyroidism was more prevalent in both T2DM groups (14, 18.7% each) compared to controls (2, 2.7%) (p value<0.004). Conclusion:Our findings strengthen the evidence of an important link between T2DM and thyroid disorders. The high prevalence of thyroid dysfunction among T2DM patients highlights the critical need for routine screening and integrated management of both conditions to enhance patient outcomes.

Magnetic resonance spectroscopy as a diagnostic model for assessment of liver steatosis in metabolic dysfunction-associated steatotic liver disease in non-diabetic patients

BackgroundMetabolic dysfunction-associated steatotic liver (MASLD) disease is the commonest hepatic cause of liver fibrosis and cirrhosis after the introduction of the direct acting antivirals and eradication of hepatitis C. MASLD is usually associated with metabolic syndrome and elevated inflammatory markers. Magnetic resonance spectroscopy (MRS) offers a non-invasive diagnostic, alternative to liver biopsy. This is a case–control diagnostic-accuracy study conducted on 40 patients in the Hepato-gastroenterology Unit in the Internal Medicine Department, Ain Shams University Hospitals, to study the role of MRI spectroscopy as a new diagnostic model for assessment of liver steatosis in non-diabetic MASLD patients compared to the standard ultrasound and clinical criteria. MASLD was diagnosed by a combination of a validated ultrasound hepatic steatosis score grading system and hepatic steatosis index using clinical and laboratory parameters. MRS was performed in all patients and fat peak, water peak, and fat fraction % were measured, and diagnostic accuracy of different MRS is compared to the US scoring and different laboratory and clinical parameters. To our knowledge this is the first study conducted on MRS in our region and Egypt.ResultsThis study revealed no statistically significant difference between the two groups regarding HbA1C, creatinine, while there was highly statistically significant difference regarding fasting blood sugar, 2 h post-prandial glucose level, urine albumin, and low-density lipoprotein levels. Hepatic steatosis score grading by abdominal ultrasound on the 20 controls showed no fatty changes with grade 0 (50%), and on the 20 MASLD patients showed that 2 cases were grade 1 steatosis (5%), 9 cases were grade 2 steatosis (22.5%), and 9 cases were grade 3 steatosis (22.5%). The diagnostic accuracy of predicting hepatic steatosis using different MRS parameters: fat peak, water peak, and fat fraction had area under the curve of 99.9%, 88.6%, and 100%, respectively. The sensitivity and specificity of fat fraction in detecting hepatic steatosis were 100%. The sensitivity and specificity of the fat peak in detecting hepatic steatosis were 100% and 95%, respectively. Moreover, the sensitivity and specificity of the water peak in detecting the hepatic steatosis were 88.6% and 85%, respectively. There is a statistically significant correlation between the three MRS parameters and the abdominal ultrasound hepatic steatosis score grades.ConclusionMRS parameters: fat fraction, fat peak, and water peak, have high diagnostic accuracy for predicting the liver steatosis. Moreover, MRS has the added advantage of being a non-invasive and a tool with low radiation risk. MRS also shows the metabolic changes in the liver and could be an eligible outcome in therapeutic clinical trials.

Inter-laboratory variation for urine albumin among laboratories in a Swedish external quality assessment scheme 2005–2023

IntroductionIncreased albuminuria is associated with elevated mortality. Urine albumin (U-ALB) above 20 mg/L or albumin-to-creatinine ratio (U-ACR) of 3 g/mol are indicative of moderately increased albuminuria. Due to limited standardization among U-ALB methods, diagnosis of increased albuminuria might prove difficult. Materials and methodsData from Equalis’s external quality assessment scheme for low U-ALB levels during 2005–2023 were categorized according to manufacturer and divided into central laboratory (CLAB) and point-of-care testing (POCT) methods. Manufacturer median values were compared to total group mean consensus values and manufacturer CV% was compared at different U-ALB levels. ResultsCLAB was generally closer to consensus values and had lower CV% than POCT at U-ALB levels around 20 mg/L. For CLAB, Roche methods were approximately equal to consensus U-ALB, Abbott 4 % above, and Siemens 5 % below. For POCT, HemoCue was 1 % below, Siemens 7 % above, and Abbott 8 % below. For U-Creatinine, all manufacturers generally had a good agreement differing on average by 1–4 % from consensus. ConclusionsAlthough U-ALB methods generally meet The National Kidney Disease Education Program (NKDEP) recommendations of method bias less than 13 % and imprecision less than 30 %, differences among manufacturers have increased over the last years, with 2023 showing the largest differences between methods. This highlights the need for guidelines for albuminuria and ACR to take method differences into consideration, but also for implementation of suitable urine reference materials.